Axonal Versus Synaptic Transmission

Concentrations of inhaled anesthetics that alter synaptic transmission typically have a smaller effect on axonal transmission, with synaptic events being about fivefold more sensitive to inhibition than impulse conduction.^[37] Nevertheless, at near-clinical concentrations, inhaled anesthetics may alter transmission through axons, and even a partial decrease in action potential propagation could decrease the amount of neurotransmitter secreted and thereby influence synaptic transmission. An apparent effect at the synapse may simply reflect depression of axonal transmission. Small-diameter axons may exhibit enhanced susceptibility to inhaled anesthetics. In the rat hippocampus, isoflurane (1.4% atm) depresses the activity of thin (0.16-mm) unmyelinated fibers but has little influence on the larger-diameter (1-mm) myelinated fibers.^[38]

The frequency at which axons transmit impulses may alter anesthetic potency. At low-impulse frequencies, volatile anesthetics produce a constant level of action potential block, whereas at relatively high frequencies, conduction block by volatile agents increases progressively. The blockade is use dependent.^[39] The branch points

Figure 4-6 Certain molluscan neurons having endogenous firing activity are extremely sensitive to volatile agents. The figure shows a continuous intracellular recording of membrane potential before, during (bar), and after exposure of a sensitive cell to normal saline solution containing halothane at a partial pressure of 0.0080 atm. (From Franks NP, Lieb WR: Volatile general anaesthetics activate a novel neuronal K⁺ current. Nature 333:662, 1988.)